An extraction algorithm for a set of elementary siphons based on mixed-integer programming

Elementary siphons are useful in the development of a deadlock prevention policy for a discrete event system modeled with Petri nets.This paper proposes an algorithm to iteratively extract a set of elementary siphons in a class of Petri nets,called system of simple sequential processes with resources (S~3PR).At each iteration,by a mixed-integer programming(MIP) method,the proposed algorithm finds a maximal unmarked siphon,classifies the places in it,extracts an elementary siphon from the classified places,and adds a new constraint in order to extract the next elementary siphon.This algorithm iteratively executes until no new unmarked siphons can be found.It finally obtains a unique set of elementary siphons and avoids a complete siphon enumeration.A theoretical analysis and examples are given to demonstrate its efficiency and practical potentials.     

Mutation of TBCE causes hypoparathyroidism-retardation-dysmorphism and autosomal recessive Kenny-Caffey syndrome

The syndrome of congenital hypoparathyroidism, mental retardation, facial dysmorphism and extreme growth failure (HRD or Sanjad-Sakati syndrome; OMIM 241410) is an autosomal recessive disorder reported almost exclusively in Middle Eastern populations. A similar syndrome with the additional features of osteosclerosis and recurrent bacterial infections has been classified as autosomal recessive Kenny-Caffey syndrome (AR-KCS; OMIM 244460). Both traits have previously been mapped to chromosome 1q43-44 (refs 5,6) and, despite the observed clinical variability, share an ancestral haplotype, suggesting a common founder mutation. We describe refinement of the critical region to an interval of roughly 230 kb and identification of deletion and truncation mutations of TBCE in affected individuals. The gene TBCE encodes one of several chaperone proteins required for the proper folding of alpha-tubulin subunits and the formation of alpha-beta-tubulin heterodimers. Analysis of diseased fibroblasts and lymphoblastoid cells showed lower microtubule density at the microtubule-organizing center (MTOC) and perturbed microtubule polarity in diseased cells. Immunofluorescence and ultrastructural studies showed disturbances in subcellular organelles that require microtubules for membrane trafficking, such as the Golgi and late endosomal compartments. These findings demonstrate that HRD and AR-KCS are chaperone diseases caused by a genetic defect in the tubulin assembly pathway, and establish a potential connection between tubulin physiology and the development of the parathyroid.